摘要
目的 :复制脂多糖 (LPS)致伤大鼠的全身炎症反应综合征 (SIRS) -肺损伤模型 ,检测肺组织IL - 1 0mRNA含量和AP - 1活性的改变 ,探讨抗炎机制在SIRS -肺损伤中的作用。方法 :梯级剂量LPS致伤Wistar大鼠 ,复制SIRS -肺损伤模型 ;逆转录PCR法 (RT -PCR)检测大鼠肺组织IL - 1 0mRNA含量 ;凝胶迁移率分析法 (EMSA)检测大鼠肺组织激活蛋白 - 1 (AP - 1 )活性。结果 :①LPS致伤大鼠 ,可以模拟SIRS -肺损伤发生 ;②LPS≥ 6mg/kg可以导致ARDS形成 ,类似SIRS失控表现 ;③LPS可以导致大鼠肺组织IL - 1 0mRNA含量和AP - 1活性升高 ;④在非失控性演进为失控性SIRS -肺损伤过程中 ,当LPS≥ 6mg/kg时 ,大鼠肺组织IL - 1 0mRNA含量和AP - 1活性的升高幅度最大。结论 :①LPS≥ 6mg/kg是大鼠SIRS -肺损伤发生失控的临界剂量 ;②大鼠SIRS -肺损伤失控伴有IL - 1 0基因转录及其调控的异常增强 ;③抗炎机制增强参与了SIRS -肺损伤发生。
AIM: To establish the model of systemic inflammatory response syndrome (SIRS)/acute lung injury (ALI) by LPS administration in rats and to measure the content of interleukin-10 massage RNA(IL-10 mRNA) and activator protein-1 (AP-1) activity in order to investigate the anti-inflammatory mechanism.METHODS: Wistar rats were injured with increased dose of LPS to set up the SIRS/ALI model. Reverse transcriptase-polymerase chain reaction(RT-PCR) and electrophoretic mobility shift assays (EMSAs) were used to measure IL-10 mRNA content and the AP-1 binding activity in rat lung, respectively.RESULTS: ①LPS could be applied to simulate SIRS-ALI in rats.②Acute respiratory distress syndrome (ARDS) could be induced under condition of LPS≥6 mg/kg, which was similar to that of the excessive expression of SIRS. ③ LPS may cause the increase content of IL-10 mRNA and AP-1 activity in lung in rat. ④Content of IL-10 mRNA and AP-1 activity were increased significantly under LPS≥6 mg/kg. CONCLUSIONS: ①LPS≥6 mg/kg might cause the SIRS/acute lung injury in rats.②The rats with excessive SIRS/acute lung injury had an obvious increase of transcription of IL-10 gene and upregulated AP-1. ③ Intensified anti-inflammatory mechanism plays a pathological role in SIRS/acute lung injury.
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
2002年第8期918-922,共5页
Chinese Journal of Pathophysiology
基金
国家自然科学基金重点项目 (No .39730 2 1 0 )
军队"十五"医学卫生课题重点项目 (No.0 1Z0 74)
